Oocyte Sensitivity to Serotonergic Regulation during the Follicular Cycle of the Teleost Fundulus heteroclitus¹

^a The Whitney Laboratory, University of Florida, St. Augustine, Florida 32086 ^b Department Anatomy and Cell Biology, College of Medicine, University of Florida, Gainesville, Florida 32610

In the teleost Fundulus heteroclitus, serotonin (5-HT) reversibly inhibits oocyte maturation induced in vitro by the maturation-inducing steroid (MIS) 17,20ß-dihydroxy-4-pregnen-3-one (17,20ßP). The 5-HT inhibition of 17,20ßP-induced meiotic maturation was examined in ovarian follicles at different developmental stages or isolated at different times during the follicular cycle. Steroid treatment of late vitellogenic and early maturing follicles (1.2- to 1.7-mm diameter) promoted oocyte maturation in a size-dependent manner, and this maturation was inhibited by 5-HT in follicles of < 1.6- to 1.7-mm diameter. Thus, the 5-HT inhibition progressively decreased as follicles developed the ability to mature in the absence of 17,20ßP. The effectiveness of 5-HT to increase follicular cAMP remained similar within the same developmental stages, indicating that the reduction of 5-HT inhibitory action was not related to the competence of 5-HT to activate inhibitory signals in the oocyte. During the follicular cycle, fully grown follicles (1.3- to 1.4-mm diameter) showed a decreased maturational competence in response to gonadotropin or MIS stimulation after the follicular recruitment into maturation and spawning occurred, which coincided with an increase of the effectiveness of 5-HT at inhibiting 17,20ßP-induced maturation. In further experiments, preincubation of follicles with hCG was found to reduce 5-HT inhibitory action, but when follicles were incubated with either hCG in the presence of a steroidogenesis inhibitor or estradiol-17ß (E₂), the 5-HT inhibition was unaffected. These findings suggest that 5-HT inhibition of the MIS-induced meiotic maturation is not under direct gonadotropin or E₂ regulation but that it might be regulated in vivo by changes in the competence of the oocytes to undergo oocyte maturation after MIS stimulation.

¹ Financial support was provided by a grant from ORTGE at UF awarded to K.S. and by an NSF grant IBN-93036123 awarded to R.A.W. Participation of J.C. was financed by a postdoctoral fellowship from the Ministry of Education and Science (Spain).

² Correspondence and current address: Division for Cell Biology (0110), German Cancer Research Center, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany. FAX: 49-6221-423404;j.cerda{at}dkfz-heidelberg.de

³ Permanent address: Department of Pharmaceutical Sciences, Nagpur University Campus, Nagpur 440010, India.

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